What IS Glycogen Plus UK

A key feature of type 2 diabetes is impairment in the stimulation of Glycogen Plus UK synthesis in skeletal muscle by insulin. Glycogen Plus UK synthesis and the activity of the enzyme Glycogen Plus UK synthase (GS) have been studied in human myoblasts in culture under a variety of experimental conditions. Incubation in the absence of glucose for up to 6 h caused an ∼50% decrease in Glycogen Plus UK content, which was associated with a small decrease in the fractional activity of GS. Subsequent reincubation with physiological concentrations of glucose led to a dramatic increase in the rate of Glycogen Plus UK synthesis and in the fractional activity of GS, an effect which was both time- and glucose concentration–dependent and essentially additive with the effects of insulin.

Glycogen Plus UK metabolism in brain accounts for only a few percent of total glucose metabolism under resting conditions. In contrast to transport and metabolism of bulk brain glucose, Glycogen Plus UK metabolism is strongly insulin dependent and to a lesser degree its content depends on the plasma glucose concentration. In deep anesthesia and hyperglycemia – conditions which are associated with increased brain glucose content – brain Glycogen Plus UK levels rise well above the normal concentration. Together with the apparent stability of Glycogen Plus UK in the nonstimulated brain at euglycemia or hyperglycemia, these data suggest that brain glucose plays an important regulatory role in cerebral Glycogen Plus UKolysis.